Not long ago, I sat on a rock near Auke Rec, watching a squadron of scoters busily diving for mussels. They weren’t doing their coordinated, follow-the-leader diving; each bird was on its own, going down to pull up a mussel.
That made me recall that spring and summer are usually the times when there are plankton blooms. Along with those events, we usually get reminders about the risks of paralytic shellfish poisoning (PSP). In fact, there was a piece in the Empire some days ago and several warnings on the radio about the unpleasant, sometimes lethal symptoms and noting that cooking does not disable the toxins. Historically, PSP has caused several episodes of multiple human deaths in Alaska.
The tiny organisms in the plankton blooms produce several kinds of toxins. Those that cause PSP are neurotoxic, affecting the nervous system (in multicellular animals that have nervous systems). Nerve impulses require the movement of sodium (and, in some cases, calcium) ions in and out of cells, and the neurotoxins impede that process. So afflicted animals can suffer numbness, paralysis, respiratory failure, and eventually death.
Plankton blooms occur when the water temperature and light are suitable and when nutrient levels are high (which commonly occurs when there is spring runoff from glaciers and freshwater streams). Among the many single-celled organisms that respond in ‘blooms’ are some that are known as dinoflagellates (referring to the whiplike ‘tail’ or flagellum that whirls to propel the cell along). There are hundreds of kinds of dinoflagellates; some are photosynthetic, some are predatory, and some are both.
Many species of dinoflagellates produce toxins of various sorts (in addition to those that induce PSP). Why do they do this? Perhaps as a means of defense against other small organisms that would eat them. Another possibility is that exposure to such toxins in the water might help a predatory dinoflagellate to capture its prey—slowing the prey’s swimming speed, perhaps immobilizing it. So the toxins are always present, but usually at low concentrations—until there is a bloom, and the toxin-producers become very abundant. A recent study showed that a particular dinoflagellate (belonging to the genus Alexandrium, which is said to be the genus most involved in toxic blooms in Alaska) increased its toxin production in response to acidified waters and low phosphorus levels, so that opens the door to potential increases in toxic blooms in the future, as ocean acidification increases (this finding should be verified by additional studies).
After watching those scoters gobbling up mussels, and thinking about the well-advertised effects of PSP on humans, I wondered about the effects of PSP on other, non-human organisms.
When there is a plankton bloom, and toxin-producing organisms are very abundant, all the numerous marine creatures that eat plankton consume vast quantities of the toxins. Many bivalve shellfish (clams, mussels, scallops, etc.) are filter-feeders, sifting plankton from the water, and they can accumulate high concentrations of the toxins. Sometimes the toxins are sequestered in certain parts of the shellfish body, such as the siphon. In some cases, the toxins may be stored for as long as two years (e.g., in butter clams), prolonging the possible effects well beyond the time of the bloom itself.
Do the dinoflagellate toxins poison the invertebrates that eat the dinoflagellates? Potentially, yes. But at least some plankton-eating invertebrates have ways of avoiding serious harm. The softshell clam, for example, develops resistance to the toxin produced by a particular dinoflagellate when it is exposed repeatedly to that toxin. This implies that the biological reason for resistance is that the toxin is damaging; otherwise, why resist? Some plankton-eaters can avoid the toxins by feeding selectively, rejecting potentially toxic dinoflagellates. For example, the Pacific oyster and the northern quahog can simply shut down feeding activity when presented with Alexandrium prey. However, this is not a direct response to the toxins themselves, but rather to the toxin-producer: even non-toxic Alexandrium strains produce the shut-down. In other cases, dinoflagellate toxins can be very damaging to larval invertebrates of several kinds. I find myself wanting to know a lot more about the physiological effects of dinoflagellate toxins on invertebrate consumers and the responses of the consumers to the presence of toxic prey.
Many marine creatures consume the plankton-eaters. Predatory snails that drill into clams or mussels can ingest toxins from the flesh of the prey. Crabs that prey on small molluscs can ingest the toxins too. Zooplankton and small crustaceans, such as krill, consume other plankton and thus become vectors for the toxins. Lots of species of small fishes consume plankton: e.g., sardines, anchovies, sand lance, herring, mackerel, young salmon. Sometimes the level of toxicity is sufficient to kill these fish, and die-offs have been recorded.
Of course, the toxins can move on up the food-chain, when the fish-eaters consume fish that have eaten toxic organisms. When the fish-eaters swallow the whole body of the prey, they obviously get the toxins even if the toxins happen to be only in the digestive tracts of the prey and not throughout the body. The concentrations of toxins tend to increase, as they move up the food-chain. There are numerous records of massive die-offs in North American waters of fish-eating marine birds (terns, gulls, pelicans, scoters, cormorants, murres, loons, etc.), and no doubt many unrecorded incidents of nonlethal illness. Marine mammals can be seriously affected too, including sea lions and humpback whales. Interestingly, sea otters are reported to able to detect the presence of PSP toxins and discard to most toxic parts, or at least just not eat so much. Butter clams are a favorite food of sea otters in some areas, and there the otters can just reject the siphon and other parts where the toxins are concentrated.